1. VT IN NORMAL AND ABNORMAL HEARTS

2. Ventricular Tachycardia Ventricular Tachycardia is Defined as Three or more consecutive PVC’s rate is usually Between 100-200 BPM Sustained VT – Episodes last at least 30 seconds/ req intervention for termination Non-sustained VT – Episodes last at least 6 beats but < 30 seconds

3. VENTRICULAR TACHYCARDIA CLASSIFICATION ECG MORPHOLOGY DURATION MECHANISM ETIOLOGY

4. Mechanisms of VT Reentrant Reentry circuit (fast and slow pathway) is confined to the ventricles and/or bundle branches Automatic – Automatic focus occurs within the ventricles Triggered activity – Early afterdepolarizations (phase 3) – Delayed afterdepolarizations (phase 4)

5. MECHANISMARRHYTHMIAEFFECT ON AUTOMATICITY-ENHANCED NORMAL ST, IDIOPATHIC VTPHASE 4 DEPOLARISATION (↓) ABNORMAL AUTOMATICITY AIVR “ TRIGGERED ACTIVITY EAD:- TORSADES de POINTES↓ AP DURATION DAD:-DIGITALIS INDUCED RVOT VT Ca ⁺⁺ overload RE-ENTRY Na⁺ channel deptSustained monomorphic VT,BB R VT, VF Ca⁺⁺ channel deptVerapamil sensitive VT

7. VT IN NORMAL HEART

8. 10% with VT - no apparent SHD Idiopathic ventricular tachycardia (VT)-SUBTYPES 1) QRS morphology 2) ventricular origin, and 3) response to pharmacologic agents management and prognosis DEF:- implies a structurally nl heart in young & middle aged subjects & a nl QT interval, although biopsy & MRI may detect subtle micro / macroscopic abnormalities

9. Synd of idiopathic VT refers specifically to monomorphic VTs. Polymorphic VTs and VF -structurally normal hearts differ from idiopathic VT -mechanistically and prognostically Commonly- subgrouped as 1)outflow tract tachycardias, 2)idiopathic left VTs (ILVTs), and 3)automatic VTs.

10. Outflow tract tachycardia outflow tract region - RV region between the pulm and tricuspid valves, - Basal left ventricle- outflow tract under the AoV, the aortic cusps, and the basal LV epicardium. A)repetitive monomorphic VT B)paroxysmal sustained VT

11. Classification by symptoms REPETITIVE MONOMORPHIC VT PAROXYSMAL SUSTAINED MONOMORPHIC VT repetitve runs of NSVT-LBBB+ N/R axisEpisodes > spread out in time Asymptomatic- incidental detection> sustained Suppressed with exerciseInducible with PES, facilitated by isoproterenol Outfow tracts of RV/LVTriggered activity Automatic mechanism Prognosis -excellent

12. delayed afterdepolarization(DAD)-mediated triggered activity - mechanism DAD- mediated by intracellular calcium overload Freq precip by catecholaminergic stimulation,↑ in intracellular cAMP and ca rapid stimulation- isoproterenol infusion. dependence on cAMP- sensitivity to β-blockade, CCB and adenosine

13. RVOT VTs -75% - LBBB+ INF AXIS -QRS transition from V₃\V₄ (late) Jadonath RL et al, localizing the origin of right ventricular outflow tract tachycardia. Am Heart J 1995 RVOT - 9 regions and used QRS morphology in leads I and aVL + R wave transition to diff ant from post RVOT sites Anterior sites- Q wave (Q or qR) in lead I and a QS in lead aVL. Posterior site- R wave in lead I and an early precordial transition( R to S) in V3 Septal- taller, narrower monophasic R-inferior leads Free wall RVOT VTs-notchi inf leads and later transition (>V3) RVOT VT-Posterior- +ve in V1, ant- -ve in V1

14. RVOT VT

17. VT arising from the LVOT (1)a) RBBB + inf axis b) dominant R wave in V1 c) lack of precordial transition d)+_a late appearing S wave in V6 and V2 (2) a) LBBB+ inferior axis+ b)early precordial R wave transition (<V₂)

18. Aortic cusps Dep on the s/o origin from the R/L cor cusp- RBBB or LBBB VT- LCC or aortomitral cont- terminal S wave in lead I Precordial transition-earlier in cusp VT (< V3) R duration & the R/S ratio V1 & V2 were > in cuspVT

20. Lcc VT

21. 9%–13% of idiopathic VT- originate from epicardial locations R amplitude was signif > inferior leads lead I had an S wave ( rS or QS pattern) Q wave ampli was >in aVL vs aVR (ratio >1.4) LV epicardial grp- 1)R wave in V1 with a > amplitude than in the RV endocardial group 2)signif S waves in V1 (>1.2 mV) and V2

22. SITE FEATURES -Ant septal side of RVOT - R/L cc of Ao -Pul artery LBBB LV- mitral annulus -epicardium at outflow tract RBBB VT with LBBB morph from LVEarly R progression( R in V1,V2,transition by V3), Dominant R across precordium VT with LBBB –RVOT/ PUL artLate R progression ( V3 or V4) Posterior septal RVOT VT> Leftward axis Free wall RVOT VTLower QRS amplitude, QRS notched in inf leads Late R wave transition V4,V5 Epicardial VT sLoss of R in V1 V2 with broad R from V3- V6

23. Outflow tract VT - good prognosis- benign course Polymorphic VT- unusually short–coupled RVOT VPCs- respond well to successful VPC ablation Management of outflow tract VTs medical therapy or catheter ablation. adenosine, verapamil, b-blockers, and carotid sinus massage-acutely b-blockers and CCBs-c/c supp therapy (efficacy 67% typical RVOT VT) Pats- breakthrough tachy on b-blocker or CCB, class I or class III antiarrhythmic therapy

24. Catheter ablation - high success rate (>80%) in treating these arrhythmias Long-term cure rates after a successful initial ablation are high overall recurrence rate is approximately 10%

25. Idiopathic left ventricular tachycardia MC-ILVT is verapamil-sensitive tachycardia 1 st -Zipes and colleagues in1979 Belhassen – demon verapamil sensitivity of the tachycardia (Response of recurrent sustained ventricular tachycardia to verapami, Br Heart J ;1981) triad: (1) induction with atrial pacing (2) RBBB morphology+ left axis deviation (3)no structural heart disease

26. 15- 40 years old. Typical symptoms palpitations, fatigue, and presyncope. Syncope and SCD are rare but described Incessant- tachycardia-induced cardiomyopathy Most episodes occur at rest( making exercise testing unreliable in assessment)

27. Anatomic basis for ILVT is unclear earliest site of activation -inferoposterior LV septum originates from a false tendon - extending from the posteroinferior LV to the basal septum localized reentry as the pred mech in verapamil- sensitive ILVT.

28. Fascicular VT - Circuit

29. Fascicular VT – Anatomy and Physiology Relatively narrow WCT 90% originate from left posterior fascicle Anatomic substrate: LV “false tendon” or postero-inferior fibromuscular band to basal septum Diagnostically – may require isoprenaline to facilitate induction Purkinje Tissue running in false tendon

30. baseline 12-lead ECG is normal in most patients. ILVT-RBBB, left sup axis + rel narrow QRS duration(≤140 ms), RS int <80 ms -exit site near the area of the left posterior fascicle ILVT-RB+ RAD –exit site near anterior fasicle

31. Three Subtypes Anatomic Origin LAHBLPHBUpper Left Septal QRS Morphology RBBB Narrow QRS AxisRightwardLeftwardNormal

33. L post fascicle- RBBB+R SUP AXIS

34. Fascicular VT – Rare mimics 1.Inter-fascicular VT RBBB and right or leftward axis Structurally abnormal heart: Previous anterior infracts and LAFB or LPFB A subtype of BBR VT 2.Idiopathic mitral annular VT RBBB and rightward axis Variable verapamil-sensitivity Ill-defined

35. Long term prognosis good A/c-iv verapamil, c/c-oral verapamil RFA- severe symptoms, resistant or intolerant to med tpy Long-term success after catheter ablation is >than 90%

36. Automatic ventricular tachycardia adrenergic or propranolol sensitive VT automaticity from within the Purkinje fibers mediated by I f result from adrenergically mediated automaticity <50 yrs, ppt by exercise Mc sites-mitral annulus,pappilary mus, RV in flo ECG - RBBB or LBBB morph and may present as monomorphic or polymorphic VT sensitive to b-blockers unresponsive to CCBs cannot be initiated with programmed stimulation

37. VT IN ABNORMAL HEART

38. CAD Incidence of sustained, monomorphic VT after infarction -3%. Modern therapy- > smaller infarcts and less aneurysm formation ---↓ incidence of VT to <1 % electrophysiologic substrate - develops in the first 2 weeks once established- remain indefinitely Once sustained VT occurs, the risk for arrhythmia continues indefinitely inducible VT signifies the presence of an anatomic VT substrate

39. PATHOPHYSIOLOGY In post MI -re-entry Areas of slow conduction -substrate for re-entry conduction is slow and discontinuous -abnormalities in gap junction distribution and function anatomic characteristics - islands of relatively viable muscle alternating with areas of necrosis and later fibrosis result in fragmentation of the propagating electromotive forces

40. MI Scar-Related Sustained Monomorphic VT Circuit

41. Sustained Ventricular Tachycardia:Role of the 12-lead Electrocardiogram in Localizing Site of Origin MARK E. JOSEPHSON, M.D., LEONARD N. HOROWITZ, CIRCULATION 1981 QRS morphology of 41 morphologically distinct VT was correlated with their site of origin as determined by catheter and intraoperative mapping. 12-lead ECG could not precisely identify the site of origin in patients with CAD Could differentiate anterior from posterobasal regions, particularly in VT -LBBB. ECG was less useful in localizing VT-RBBB because of overlapping patterns General QRS patterns were useful in differentiating anterior from posterior regions of origin

42. LOCUSFINDINGS APICALQ in L 1, V2 &V6(all Three Leads) BASALR in L1,V2 & V6 POSTEROBASALPOSITIVE PRECORDIAL CONCORDANCE SUPERIORINFERIOR AXIS (NL OR RIGHT) INFERIORSUPERIOR AXIS (LEFT OR NORTHWEST)

43. RBBB & LBBB VT- ANTERIOR

44. RBBB & LBBB VT -POSTERIOR

46. q wave in lead 1 and/or V6 - RBBB – anteriorly

47. RBBB-FROM ANTEROLATERAL LEFT VENTRCLE

48. R in leads L1 and V1 through V6, in RBBB specific for a posterior origin

49. Electrocardiograrm During Ventricular Tachycardia with Left Bundle Branch Morphology

50. LBBB pattern+ Q waves in leads I and V6 -anterior superior and leftward axis - inferior aspect of septum.

51. LBBB+ q in L1,V6-ant inferior & rightward axis - superior septum

52. LBBB-POSTEROBASAL LV -R in L1,V2,V3& V6

53. JM Miller ;Circulation 1988;, Relationship between the 12-lead ECG during VT and endocardial site of origin in patients with coronary artery disease Endocardial mapping - 182 VTs in 108 patients with prior AW/IW MI Endocardial sites of origin -identified with use of catheter or intraoperative activation mapping ECGs - 4 features a)location of infarction,b) BBB type c) axis d) precordial R wave prog pattern specific combination- 4 features- particular endocardial origin in 87 VTs (48% of total) An asso (> 70% ppv) 1)left> right, BBB type (73% vs 31%) 2) VT related to inf > ant infarction ( 74% vs 37%).

54. PRECORDIAL LEADS IN LOCATING VT ANTERIOR WALL MI INFEROAPICAL SEPTAL FOCUS V1 NEGATIVE + LAD + NO LATE R PROGRESSION ANTEROSUPERIOR APICAL SEPTAL FOCUS V1 NEGATIVE + INF AXIS (NL/R) ANTEROAPICAL SEPTAL FOCUS V1 POSITIVE + RAD + ABRUPT LOSS OF PRECORDIAL PROGRESSION INFERIOR MI INFEROBASAL SEPTAL FOCUS V1 NEGATIVE + LAD + GROWING R PROGRESSION INFEROBASAL FREEWALL FOCUS V1 POSITIVE +SUP AXIS + REVERSE LATE R PROGRESSION MIDPOSTERIOR SEPTAL FOCUS V1 NEGATIVE + INF RIGHT AXIS + REVERSE (early/late)R PROGRESSION

55. Regions are: A, inferoapicalseptum; B, anteroapical septum; C, anteroapical free wall; D, anterobasal free wall; E, anterobasal and midseptum; F, inferobasal septum; G, inferomedial free wall; H, inferolateral free wall; I, midinferior J, inferoapical free wall. G + H =inferobasal free wall.

57. Algorithm developed with the above criteria was applied prospectively to 110 VTs (all mapped) in 63 patients algorithm could correctly predict endocardial region of origin for a mean of 60 of 65 (93%) VT

58. ANTERIOR INFARCTION-VT

59. INFERIOR INFARCTION -VT

60. INFARCTIO N SITE OF ORIGIN VT TYPE JOSEPHSON’S MILLERS ANTERIORINFEROAPICA L LBBB q –L1, V6 SUP± LAD Poor R Progression/ no or late progression ANTEROAPIC AL LBBB q –L1,V6 INF AXIS Any precordial prog ANTEROAPIC AL RBBB q –L1&/ V6 INF AXIS Dominant R / abrupt loss INFERIORINFEROBASA L LBBB R –L1,V2,V3&V6 SUP ± LAD Growing R pattern INFEROBASA L RBBB R-L1,V2,V3&V6 SUP ± LAD Reverse R prog- late /early INFEROLATER AL RBBB R-L1,V2,V3,V6 INF AXIS Late reverse R prog

61. Ventricular arrhythmias in the setting of coronary artery disease all available antiarrhythmics except Amiodarone, l-Sotalol and Dofetilide increase mortality in the post MI population

62. Secondary Prevention of SCD survivors of SCD or sustained VT- ICD provides the lowest mortality.

63. Primary Prevention of SCD in Ventricular Arrhythmias a prior MI, dec EF and NSVT -ICD provides the lowest mortality. a prior MI, dec EF and NSVT -ICD provides the lowest mortality.

64. Primary Prevention of SCD in absence of Ventricular Arrhythmias patients with significant LV dysfunction - best survival with ICD patients with significant LV dysfunction - best survival with ICD

65. Goal of longterm therapy-a) pvt of SCD, b) Rec of symp VT After MI Asymptomatic NSVT in pats with NLVEF- no treatment Symptomatic NSVT in pats with NLVEF- betablockers NSVT in red LVEF-↑ SCD PRIMARY PVT - ICD > AMIOD- pvt of SCD SECONDARY PVT- Class lll > l - emperical amio > than EP guided antiarry’s - ICD > amio in LVEF<35% SCD/SUS VT in ↓LVEF- ICD CAD-NL LVEF + SUST VT-?, amio, icd + amio, RFA

66. Macro re-entrant (→Ventricular flutter) circuit employing… – Both bundle branches – Ramifications of the left bundle Hallmark: His-Purkinje system disease – functional or structural Acquired heart disease or apparently normal hearts Ischemic (6%) vs. non-ischemic (40%) cardiac disease Bundle Branch Re-Entry Ventricular Tachycardia

67. LB Catheter RB Catheter V Catheter His Catheter VT QRS Morphology Activation Sequence LBBBH-RB-V-LB RBBBH-LB-V-RB

68. VT Due to Bundle Branch Reentry

70. VT incorporating both bundle branches into the reentry circuit usually in an acquired heart disease and significant conduction system impairment Reentry within HPS in humans was first documented by Akhtar et al 1974 sustained bundle branch reentry can not be induced in patients with normal HPS. Nl- very fast conduction velocity and a relatively long refractory period which precludes formation of a stable reentry circuit Persistent BBR as a mechanism of sustained VT has been demonstrated in patients with conduction system impairment

71. Dilated cardiomyopathy -non-ischemic- 40% Vs ischemic - 6% Aortic or mitral valve surgery Close anatomical proximity of the HPS to the valvular annuli early postoperative period ( first 2 weeks) preserved systolic left ventricular function Myotonic myocardial dystrophy characterized by relatively selective and significant conduction system impairment idiopathic isolated conduction system disease

72. Surface ECG in sinus rhythm - non-specific or typical bundle branch block patterns with prolonged QRS duration Total interruption of conduction in one of the BB would theoretically prevent occurrence of reentry “complete” BBB -not an accurate marker of complete conduction block Can occur in patients with relatively narrow QRS complex - functional conduction delay

73. presyncope, syncope or sudden death - VT with fast rates > 200 bpmleft LBBB pattern-mc VT morphology VT of myocardial origin vs BBR-LB pattern – rapid intrinsicoid deflection - initial ventricular activation through the HPS BBR -LBBB -antegrade direction -RB & reterograde LB BBR –RBBB- antegrade direction-LB & reterograde RB

74. Prolonged H-V interval in sinus rhythm Fig 2

75. INTERFASCICULAR REENTRY TACHYCARDIA usually has RBBB morphology Antegrade - LAF & retro – LPF –RAD Antegrade- LPF & retro – LAF- LAD Fig 3

76. Pharmacologic therapy- empiric and EP guided - ineffective RFA - first line therapy choice is ablation of the RB

77. ARVC Ind JH et al. Indian Pacing Electrophys J. 2003:3:148 – Fibro-fatty replacement of the myocardium – Thin and enlarged RV wall. – Trichrome stain – Areas of mature fibrosis (F) and adipose tissue (A) within the epicardial (Epi) and mid- myocardial zones

78. Arrhythmogenic Right Ventricular Cardiomyopathy - ARVC

79. Major Conduction abnormalities – Epsilon waves in V1 - V3 – Localized prolongation (>110 ms) of QRS in V1 - V3 MINOR – Inverted T waves in V2 and V3 in an individual over 12 years old, in the absence RBBB – Late potentials on SAECG – Ventricular tachycardia with a LBBB morphology – Frequent PVCs (> 1000 PVCs / 24 hours)

80. ARVD Ventricular arrhythmias are usually exercise- related sensitive to catecholamines. right axis deviation,LBBB Multiple morphologies of ventricular tachycardia multiple foci or pathways.

81. ARVC High Risk Features Younger patients Recurrent syncope History of cardiac arrest or sustained VT Clinical signs of RV failure or LV involvement Patients with or having a family member with the high risk ARVD gene (ARVD2) Increase in QRS dispersion ≥ 40 msec – QRS dispersion = max measured QRS minus min measured QRS Naxos disease

82. Sotalol Catheter ablation – treat intractable ventricular tachycardia – 60-90% success – recurrence is common (60% recurrence rate) – drug-refractory VT – frequent recurrence of VT causing frequent discharges of the ICD.

83. VT MONOMORPHIC POLYMORPHIC RBBB LBBB STRUCTURALLY NL HEART STRUCTURALLY ABNORMAL HEART

84. RBBB NORMAL HEART Outflow tract VT mitral annulus, epicardium of out flow Ao mitral cont ILVT - RAD- LAF - LAD – LPF AUTOMATIC / PROP SEN ABNORMAL HEART POST MI - septum/free wall- inf - apex- sup + RAD BBR VT - ante LB -retro-RB FASCICULAR VT - RAD –ante –LAF - LAD – ante - LPF

85. LBBB NORMAL HEART OUTFLOW TRACT VT - RVOT - LV SITE OF THE SEPTUM AUTOMATIC / PROP SENS ABNORMAL HEART POST MI ARVD UHL’S ANOMALY POST SX –TO DCM - LV VT -BBR VT ante-RB.retro-LB